Strength training attenuates post-infarct cardiac dysfunction and remodeling.

Post-myocardial infarction (MI) exercise has been employed to improve cardiac function. However, most studies have focused on endurance training (Et). Although Et has been reported to preserve cardiac function, evidence suggests that Et increases left ventricle (LV) interior dimensions as a result of albumin-induced plasma expansion. In contrast, strength training (St) induces concentric cardiac hypertrophy and improved cardiac function without causing ventricular dilation. Therefore, the purpose of this study was to investigate the effects of St on cardiac function and remodeling in rats with MI. MI was surgically induced in 7-week-old rats via ligation of the coronary artery. Survivors were assigned to two experimental groups, MI-Sed (No exercise; n = 9), MI-St (St; n = 10), with a Sham group (no MI, no St; n = 9). MI-St rats began training 1-week post-MI by climbing a ladder with weights for 10 weeks. Echocardiographic measurements were performed prior to, and following exercise training, while in vivo LV hemodynamic analysis was conducted at the end of the experimental period. Our data revealed that St induced shortening of the LV end-diastolic dimension in the MI-St group compared with the MI-Sed group (P < 0.05). The peak velocities of contraction (+ dP/dt max) and relaxation (- dP/dt max) were significantly greater in the MI-St group than the MI-Sed group (P < 0.05). These training effects contributed to the improved fractional shortening (%FS). Our results demonstrate that St may be beneficial for post-MI by attenuating LV dilation and concomitant cardiac dysfunction associated with MI.

Post-myocardial infarction exercise training beneficially regulates thyroid hormone receptor isoforms.

Thyroid hormone receptors (TRs) play a critical role in the expression of genes that are major determinants of myocardial contractility, including α-myosin heavy chain (α-MHC) and ß-MHC. After myocardial infarction (MI), changes in myocardial TRs consistently correlate with changes in thyroid hormone (TH) target gene transcription, and this is thought to play a key role in the progression to end-stage heart failure. Interestingly, post-MI exercise training has been shown to beneficially alter TH-target gene transcription and preserve cardiac function without changing serum TH. Therefore, in this study, we investigated whether mild exercise training alters expression of α1 and ß1 TR isoforms in post-MI rats. Seven-week-old male Sprague-Dawley rats underwent coronary ligation or sham operation, and were assigned to 3 groups (n = 10): sham, sedentary MI (MI-Sed), and exercise MI (MI-Ex). Treadmill training was initiated 1 week post-MI, and gradually increased up to 16 m/min, 5° incline, 50 min/day, 5 days/week, and lasted for a total of 8 weeks. Real-time polymerase chain reaction and gel electrophoresis were performed to quantify changes in TR isoforms. Our results illustrated that mRNA expression of TR-α1 and TR-ß1 was higher in both MIs; however, protein electrophoresis data showed that TR-α1 was 1.91-fold higher (P < 0.05) and TR-ß1 was 1.62-fold higher (P < 0.05) in the MI-Ex group than in the MI-Sed group. After MI, TR-α1 and TR-ß1 protein levels are significantly decreased in the surviving non-infarcted myocardium. Moderate-intensity exercise training significantly increases TR-α1 and TR-ß1 protein expression, which in turn may upregulate α-MHC and improve myocardial contractile function and prognosis.

Cardiac remodeling and physical training post myocardial infarction.

After myocardial infarction (MI), the heart undergoes extensive myocardial remodeling through the accumulation of fibrous tissue in both the infarcted and noninfarcted myocardium, which distorts tissue structure, increases tissue stiffness, and accounts for ventricular dysfunction. There is growing clinical consensus that exercise training may beneficially alter the course of post-MI myocardial remodeling and improve cardiac function. This review summarizes the present state of knowledge regarding the effect of post-MI exercise training on infarcted hearts. Due to the degree of difficulty to study a viable human heart at both protein and molecular levels, most of the detailed studies have been performed by using animal models. Although there are some negative reports indicating that post-MI exercise may further cause deterioration of the wounded hearts, a growing body of research from both human and animal experiments demonstrates that post-MI exercise may beneficially alter the course of wound healing and improve cardiac function. Furthermore, the improved function is likely due to exercise training-induced mitigation of renin-angiotensin-aldosterone system, improved balance between matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-1, favorable myosin heavy chain isoform switch, diminished oxidative stress, enhanced antioxidant capacity, improved mitochondrial calcium handling, and boosted myocardial angiogenesis. Additionally, meta-analyses revealed that exercise-based cardiac rehabilitation has proven to be effective, and remains one of the least expensive therapies for both the prevention and treatment of cardiovascular disease, and prevents re-infarction.

Exercise training induced myosin heavy chain isoform alteration in the infarcted heart.

The myosin heavy chain isoform MHC-α has 3-fold higher ATPase activity than MHC-ß. After myocardial infarction (MI), MHC-α expression is profoundly downregulated and MHC-ß expression is reciprocally upregulated. This shift, which is attributed to low thyroid hormone (TH), contributes to myocardial systolic dysfunction. We investigated the effect of post-MI exercise training on MHC isoforms, TH, and cardiac function. MI was surgically induced in 7-week-old rats by ligation of the coronary artery. The survivors were assigned to 3 groups (n = 10/group): Sham (no MI, no exercise), MISed (MI, no exercise), and MIEx (MI, exercise). Treadmill exercise training began 1 week post-MI and lasted for 8 weeks. Echocardiogram measurements were taken on the day prior to initiation of exercise training and at the end of exercise training. Tissue and blood samples were collected at the end of the experiment. MHC isoform gene and protein expression and TH were measured. Our results illustrated that MHC-α gene expression was higher and MHC-ß gene expression was lower in the MIEx group than in the MISed group. Resting serum TH concentrations (T3 and T4) were similar between the 2 MI groups. The MIEx group had higher fractional shortening than the MISed group. In conclusion, post-MI exercise training beneficially altered MHC isoforms and improved cardiac function without changing TH.